Chapter 22 Flashcards
Pathogens
harmful disease causing agents
Bacteria
-Single celled
-composed of prokaryotic cells
Virsues
Not cells they are very small and contain DNA and RNA in protein capsules and must enter a cell
Fungi
composed of eukaryotic cells that have a cell wall external to the plasma membrane
Protozoans
microscopic unicellular eurkaryotic
organisms that lack a cell wall
-Intra or extracellular
-This enters the blood
Prions
small fragments of proteins that cause disease in nervous tissue
Innate immunity
-what you are born with. IT provides multiple components that protect against a wide array of substances
1st line of defence
Skin and mucosal membrane (prevent entry)
2nd line of defence
Nonspecific internal defenses
-Immune response (ex macrophages, NK cells)
-Chemical (inferno or complement)
-Physiologic responses (inflammation)
-Plasma membrane
Skin
-1st defense
-Physical barrier of epidermis & dermis
-Sweat & sebaceous glands release antimicrobials
-importance evident with burn victim
Mucous membrane
-line body openings
-Mucus and antimicrobial secretions (Defensins, lysozyme, IgA , acid)
-Various other mechanisms and secretions in different body areas (cilia and resp)
Defensins
small cysteine-rich cationic proteins across cellular life, including vertebrate and invertebrate animals, plants, and fungi. They are host defense peptides, with members displaying either direct antimicrobial activity, immune signaling activities, or both.
lysozyme
protein present in many mucosal secretions (tears, saliva, and mucus) and tissues of animals and plants, and plays an important role in the innate immunity, providing protection against bacteria, viruses, and fungi.
Selected immunity
- Phagocytes (neutrophils, macrophages, dendritic cells)
Apoptosis-initiating (NK cell)
Parasite-destroying (eosinophils)
Proinflammatory chemical-secreting (basophils, mast cells) - Inflammation
- Antimicrobial proteins (inferons)
- Fever
Phagocytes include
-Dendritic cell
-infectious agent engulfed
-Macrophages
-Phagosomes
-Lysosomes
-Phagolysomes destroy infectious agent
-They engulf foreign substances
Dendritic cells
Antigen presenting cells that phagocytose pathogens & display antigens on their surface that are recognized by T cells (adaptive)
Selected Immune cells: NK cells
Circulate in blood and accumulate in 2nd lymphoid structures
Selected immune cells: parasite destroying
Degranulate & release cytotoxic chemicals that create pores in parasite cells
Selected immune cells: Pro-inflammatory chemical secreting
-Chemical alarm
-Vasodilation goes up, local blood flow goes up
-FLuid clotting factors exudate
-Increased movement of fluid from blood to injury tissue
-Increased chemotaxis to attract immune cell decrease inflammation
Chemotaxis
Refers to the directional migration of cells in response to chemical gradients
Histamine source
mascells and basophil granules
Histamine physiological effects
Vasodilation of local arterioles = increased blood flow
Permeability of local capillaries = increased exudate (fluid with clotting factors & antibodies)
Chemotaxis of leukocytes
Prostaglandins, leukotrienes source
Produced from a component in all cell membranes by actions of neutrophils, basophils & others
Prostaglandins, leukotrienes effect
Vasodilation of local arterioles = increased blood flow
Permeability of local capillaries = increased exudate (fluid with clotting factors & antibodies)
Chemotaxis of leukocytes and increased pain
kinins (bradykinin) source
Precursor protein is cut by enzyme in saliva, plasma, urine & neutrophils to become active kinins
Kinins effect
Vasodilation of local arterioles = increased blood flow
Permeability of local capillaries = increased exudate (fluid with clotting factors & antibodies)
Chemotaxis of leukocyte and increased daub and chemotaxis creates more kinins
Complement proteins source
Blood
Complement protein effect
O-ICE:
Opsonization increases phagocytosis
Intensifies inflammation
Cytolysis lyses pathogens
Elimination of antibody complexes aids in the adaptive immune response
Cytokines (see slide 46 for details)
Interferons (IFNs)
Interleukins (ILs)
Colony-stimulating factors (CSFs)
Tumor necrosis factors (TNFs)
(source)
Many cells including T-cells, dendritic cells & macrophages
Cytokines (see slide 46 for details)
Interferons (IFNs)
Interleukins (ILs)
Colony-stimulating factors (CSFs)
Tumor necrosis factors (TNFs)
Enhances inflammation
Mainly involved in cell-mediated (T-cell) adaptive immunity
Four cardinal signs of Inflammation
Redness: increased blood flow
Heat: Increased blood flow and metabolic activity
Swelling: Increase fluid loss from capillaries to tissue
Pain: Pro-inflammatory chemical activation of complement and compression due to increased fluid
CAM
Cell adhesion molecules
Inflammation step 1
- release of inflammatory and chemotactic factors
Inflammation step 2
Vascular changes
-vasodilation of arterioles
-increase in capillary permeability
-Display of CAMS
Inflammation step 3
Recruitment of leukocytes
-magination
-Diapendesis
-chemotaxis
Stick, squeeze, scoot
Fluid clotting
Antimicrobial proteins: Complient system
Increase inflammation, elimination of immune capsule, opsonization, cytolysis
How does Increased inflammation happen
Mast cells, basophils, neutrophils and macrophages
What is the purpose of a fever
-mobilizes defences accelerates repairs inhibits pathogens
-Increased metabolic rate to speed healing
-Inhibit bacterial growth
Levels of fever
Low-grade: 38-38.3oC
Intermediate grade: 38.8oC
High-grade: 39.4-40oC;
Dangerous high-grade: >40oC
T Lymphocytes
Effective against antigens within cells regulate antigen presenting cells
Cytotoxic T Lymphocytes
involved in directly killing intracellular pathogens and eliminating mutated and cancerous cells
B lymphocytes
(provide antibody mediated immunity) effective antigen outside cells does not require antigen presenting cells
Adaptive vs Innate
Adaptive has
1. Specificity (response to Ag)
2. Uses lymphocytes (Many different lymphocytes each specific for particular ag)
3. has memory (activation, clones, memory, fast)
4. Is systemic (not restricted to site of injury circulation in blood lymph
Antigens are
self generating
Any substances that can mobilize adaptive defenses
Usually a protein or large polysaccharide not normally found in the body
Foreign antigens
bind immune components (Different from body molecules)
Self antigens
Do not bind immune components
(Own nodes molecule)
Autoimmune disorder
Immune system reacts self as if it was foreign
Immunogenicity
ability of an antigen to trigger lymphocyte proliferation (multiplication)
Hapten
small molecule that cannot be an antigen on its own, bind to self protein become immunogenic and harmful
Antigenic determinant
-also known as an epitope= specific site on antigen recognized by receptors on immune cells.
-Each has a different shape
-Pathogens can have multiple determinants
-can be recognized by many antibodies
Self-Antigens & Major Histocompatibility (MHC) Proteins
MHC proteins are one of many that identify a cell as self
-have genetically determined structure that is unique to individual
-MHCs can bind either a self or foreign antigen & display it on the cell surface
Lymphocytes Life cycle
- formation
- Maturation
- seeding
- Antigen encounter and activation
- Proliferation and differentiation
Who does T cells bind to
T-cells can only bind antigens that are presented to them on MHC proteins
Lymphocyte Maturation
-Educated as they mature
-Immunocomptence becomes able to recognize one specific antigen
-Self tolerance is unresponsive to self antigens
Lymphocyte Formation
B & T-cells originate in red bone marrow
Lymphocyte Seeding (colonization)
Immunocompetent, naïve B & T-cells seed the 2nd lymphoid
-circulate to increase chance that they will find their antigen
Antigen encounter and activation
Antigen binding selects that cell for further development = clonal selection
-activation if signal are present
Lymphocyte proliferation and differentiation
-Lymphocytes multiply rapidly once activated making identical clones of itself
-Most become effector lymphocytes and do the work
-Some become memory lymphocytes and circulate constantly “patrol”
Antigen Presenting cells (APCs)
Dendrite, macrophages, B lymphocytes
Dendrite cells
Found at body’s frontiers
Internalize pathogens & migrate to Lymphnodes
Most important way of ensuring T-cells encounter antigens
Macrophages
-there is a wide distribution they engulf and eliminate infected cells
B-Lymphocytes
-Cannot activate naive T cells
-Can only present to helper Cells to assist in their own activation
Humoral Immunity Primary response
100 000 receptor cells
activated B cells
Plasma cells (effector B)
Secreted antibodies
antigens binds to receptors on V cell
Proliferation to form clots
Memory B cells primed to respond to same antigen
Humoral secondary response
(could be years later)
Clone of the cell indexical to ancestor
Subsequent challenges by same antigen results in large fast response
Active Immunity
-Production of memory cells due to contact with antigens
Primary and Secondary Response
Primary: 3-6 days activation, proliferation, differentiation into plasma cell
Secondary: Lower (shorter) lag time due to memory B cells
Naturally Acquired active immunity
-Direct exposure to antigen following entry of the pathogens into the body naturally
Articfically acquired Active immunity
Antigen exposure from vaccine
Passive immunity
-No production of memory cells, antibodies from another person or an animal
Naturally acquired passive immunity
transfer is mother to child across the placenta or breast milk
Artificially acquired passive immunity
Transfer of serum containing antibody from another person or animal (Rabies vaccine, snake venom antibodies)
Antibody
immunoglobulin (Ig) proteins produced against a specific, soluble antigen (i.e., those in the blood & lymph)
Antibody structure
4 polypeptide chains
Variable region, constant region,
Immunoglobulin classes
IgM, IgA, IgD, IgG, IgE (MADGE)
IgM
(pentamer)
B-cell antigen receptor
First antibody produced during primary response
Readily activates complement
Potent agglutinating agent
Only fetal antibody
IgA
Secretory IgA in body secretions – sweat, saliva, intestinal juice, milk
Stops pathogens from attaching to mucous membranes & epidermis
(DIMER)
IgD
Monomer
(B cell antigen receptor)
IgG
Monomer
Most abundant antibody in plasma (75-85%)
Main antibody of secondary response
Readily activates complement
Can cross placenta – passive immunity to fetus
IgE
Monomer
Stem binds to mast cells & basophils
Antigen binding triggers release of chemicals from granules – histamine etc.
Levels rise during severe allergic reactions
Neutrolization
Antibody covers biologically active portion of microbe or toxin
Agglutination
(elimination of bacteria) Antibody cross-link cells forming a clump. Easier for phagocytes to see and eat
Precipitation
Antibody cross-links circulating particles forming an insoluble antigen-antibody complex
Antibody targets and functions
Antigen-antibody complexes inactivate targets & tag them for elimination by innate immune and adaptive system
-3 are due to Antigen-antibody binding
-3 are due to exposure of Fc region after antigen-antibody binding
-
Opsonization
Fc region of antibody binds to receptors of phagocytes cell triggering phagocytosis
Complement fixation
Fc region of antibody binds complement proteins complement is activated
Activation of NK cells
Fc region of antibody binds to an NK cell, triggering release of cytotoxic chemicals
Types of T cells and function
CD4 Helper Cell (Th)
-Helps activate B cells, Cells, macrophages, innate immune system
-Releasing cytokines
(don’t fear If any villain dare invade I will come to the rescue)
and
CD8 Cytotoxic (killer) T cell (Tc) Kill apoptosis perforin granzymes (find and kill)
Major categories of Cytokines
Interleukin, Tumor necrosis factor, Colony stimulating factor, interferon
Released from one cell & bind to receptors of target cells
Cell that released it (autocrine)
Local cells (paracrine)
Distant cells after circulating through blood (endocrine)
Have short half-life
Interleukin (IL)
-regulates immune cells, T-lymphocytes, macrophages, endothelial cells and other various cells
-IL followed by a number
Tumor necrosis factor (TNF)
Destroys tumour cells, T-Lymphocytes, macrophages, mast cells, dendritic cells
TNF followed by a greek letter
Colony stimulating factor
Stimulates leukopoesis in bone marrow to increase synthesis of a specific type of leukocytes
first letter and then followed by CSF
Inferons
Interferes with replication of pathogens that enter cells
-infected cell, NK cells, T-Lymphocytes
-IFN followed by a greek letter
Response of CD4 Helper Lymphocyte
- first signal CD4 binds with MHC class II molecule of APCc, TCR interacts with antigen within MHC class II molecule
-Activated helper T Lymphocytes form a clone of activated and memory helper T Lymphocytes
IL 2 released from helper TLymphocutes bind to promote proliferation
